Pulmonary artery hypertension (PAH) is a female dominant, fatal disease characterized by progressive increase of pulmonary vascular resistance and loss of compliance. The role of estrogen in these pulmonary vascular changes with PAH progression remains unclear. Our objective was to study the effects of estrogen on pulmonary arterial (PA) remodeling in a mouse model of progressive PAH, created via a combination of a VEGF inhibitor Sugen and chronic hypoxia (SuHx). To quantify PA hemodynamics, we measured in vivo pressure and flow simultaneously in live mice in order to obtain pulmonary vascular impedance, a comprehensive measure of RV afterload. Our results demonstrate that estrogen modifies the relationship between PA resistance and compliance by attenuating PA stiffening, which provides insight into sex differences in PAH progression.

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